Recent research in mice with age-related hearing loss has established that an augmented acoustic environment (AAE) consisting of moderate-level pulsed noise bursts presented for 12 hrs per day can, as measured by auditory brainstem responses (ABRs) and spiral ganglion-cell counts, dramatically retard the functional and histological changes typically associated with such genetically-based accelerated aging processes. Whether these ameliorating influences also disrupt the associated degeneration of sensory receptor cells has not yet been determined. The primary goal of the proposed study is to assess to what extent, if any, an AAE affects the progressive sensory-cell loss in mice that exhibit rapid-onset presbycusis. This aim will be accomplished using functional and histological methods in two strains of mice, consisting of the prematurely aging C57s and the normal CBAs, by, respectively, monitoring distortion-product otoacoustic emissions (DPOAEs) that reflect the normal micromechanical activity of outer hair cells (OHCs), and evaluating hair-cell presence in plastic-embedded whole mounts of the cochlea. The C57 strain shows progressive sensory-cell degeneration that is advanced by age 6 mo, whereas the CBA strain exhibits normal cochlear function and sensory-cell presence up to age 18 mo. The planned experiments will determine if DPOAEs and cochlear histopathology in the C57s differ in an experimental group exposed to an AAE as compared to the identical measures obtained for control C57s housed under normal vivarium conditions. The outcome of the AAE treatment will also be compared to similar groups of CBA mice, which are not expected to show any changes as a result of exposure to the same acoustically enriched environment or vivarium conditions. ABRs will also be obtained in order to facilitate comparisons of these findings to the earlier results as well as to determine if they improve in the absence of significant AAE-induced cochlear effects. The finding that an AAE can preserve OHC function and prevent or retard hair-cell degeneration would have far-reaching implications for plasticity of auditory sensory receptors, and indicate that the adverse effects of certain genetic forms of hearing loss can be deliberately reversed.